Abstract

Anopheles mosquitoes are the primary vectors for malaria in Africa, transmitting the disease to more than 100 million people annually. Recent functional studies have revealed mosquito genes that are crucial for Plasmodium development, but there is presently little understanding of which genes mediate vector competence in the wild, or evolve in response to parasite-mediated selection. Here, we use population genetic approaches to study the strength and mode of natural selection on a suite of mosquito immune system genes, CTL4, CTLMA2, LRIM1, and APL2 (LRRD7), which have been shown to affect Plasmodium development in functional studies. We sampled these genes from two African populations of An. gambiae s.s., along with several closely related species, and conclude that there is no evidence for either strong directional or balancing selection on these genes. We highlight a number of challenges that need to be met in order to apply population genetic tests for selection in Anopheles mosquitoes; in particular the dearth of suitable outgroup species and the potential difficulties that arise when working within a closely-related species complex.

Highlights

  • Mosquitoes belonging to the Anopheles gambiae Giles species complex include the primary vectors of human-pathogenic Plasmodium species in sub-Saharan Africa, and as such are indirectly responsible for the deaths of more than one million people annually (World Malaria Report, WHO 2005)

  • We were able to amplify all loci from five species of the An. gambiae complex (An. gambiae s.s., An arabiensis, An. merus, An. bwambae and An. quadriannulatus), with the exception of ‘housekeeping’ locus ENSANGG00000019219 from An. bwambae

  • This study used DNA polymorphism and divergence data to test whether mosquito immunity genes thought to be important for Plasmodium development might be subject to host-pathogen arms races or balancing selection

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Summary

Introduction

Mosquitoes belonging to the Anopheles gambiae Giles species complex include the primary vectors of human-pathogenic Plasmodium species in sub-Saharan Africa, and as such are indirectly responsible for the deaths of more than one million people annually (World Malaria Report, WHO 2005). This has driven research into the molecular basis of mosquito–Plasmodium interaction, most notably the sequencing of the An. gambiae genome (Christophides et al 2002; Holt et al 2002) and the subsequent identification of genes that mediate mosquito susceptibility to Plasmodium infections

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